In his best-selling 2011 book entitled “Thinking Fast and Slow”, Nobel laureate Daniel Kahneman elucidates the contrast between two modes of human thought-processing: fast and slow thinking.1 Fast thinking is characterized by rapid and automatic reaction to a simulation or problem, while slow thinking involves a measured and analytical response. This dichotomy epitomises the clash between clinicians and basic scientists on the enigma of anaesthetic neurotoxicity.2 Based on their clinical practise that anaesthetics do not overtly produce neurocognitive deficits, the clinician’s viewpoint relies on instinct and experience, while the scientist’s viewpoint is based on a deliberate analysis of experimental data and its logical extrapolation to the clinical setting.
- Increasing the interval between repeated anesthetic exposures reduces long‐lasting synaptic changes in late post‐natal mice
- Tau Contributes to Sevoflurane-induced Neurocognitive Impairment in Neonatal Mice
- Neonatal exposure to sevoflurane expands the window of vulnerability to adverse effects of subsequent exposure to sevoflurane and alters hippocampal morphology via decitabine-sensitive mechanisms
- Sevoflurane Post-Conditioning Ameliorates Neuronal Deficits and Axon Demyelination After Neonatal Hypoxic Ischemic Brain Injury: Role of Microglia/Macrophage
- Behavior and Regional Cortical BOLD Signal Fluctuations Are Altered in Adult Rabbits After Neonatal Volatile Anesthetic Exposure